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Reprinted  from  the  ‘Reports  of  the  Society  for  the  Study  of  Disease  in 
Children ’ VoL  I,  1901. 


A CASE  OP  PNEUMOCOCCAL  PERITONITIS. 

By  J.  H.  BRYANT,  M.D. 

Harriet  S — , aged  four  years,  was  admitted  into  Guy’s 
Hospital  under  my  care  on  May  the  11th,  1901,  for  vomit- 
ing and  abdominal  pain.  She  had  always  enjoyed  good 
health  until  the  evening  of  May  the  9tli,  when  she  was 
seized  with  severe  vomiting  after  supper.  She,  vomited 
about  six  times  during  the  night.  The  sickness  ceased  on 
the  following  morning,  but  she  appeared  to  be  very  ill,  and 
would  not  take  her  food.  On  the  morning  of  the  11th, 
as  she  was  much  worse,  and  had  not  taken  any  food,  she 
was  brought  up  to  the  hospital,  and  was  at  once  admitted. 
She  had  not  been  sick  since  the  evening  of  the  9th. 
The  bowels  were  opened  on  the  10th,  and  the  motion 
appeared  to  be  natural.  There  was  no  discharge  of 
blood  or  mucus  from  the  rectum. 

On  admission  the  pulse  was  140  to  the  minute,  the 
temperature  102-8°  F.,  and  the  respirations  40  to  the 
minute.  She  appeared  to  be  vei’y  ill,  and  had  a drawn 
and  anxious  expression.  The  abdomen  was  tense,  rigid, 
and  very  tender  all  over.  There  was  no  particular  pain  or 
tenderness  in  the  right  iliac  fossa.  There  were  no 
physical  signs  of  pleurisy  or  pneumonia.  I saw  the  child 
soon  after  admission,  and  came  to  the  conclusion  that  she 
Avas  suffering  from  acute  peritonitis  or  diaphragmatic 
pleurisy,  and  I suggested  the  possibility  of  a pneumo- 
coccal infection  on  account  of  the  absence  of  any  localising 
symptoms  of  appendicitis  or  other  diseases.  Mr.  Dunn 
saAv  the  child  with  me  shortly  afterwards,  and  decided 

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PNEUMOCOCCAL  PERITONITIS. 


not  to  operate,  chiefly  on  account  of  the  absence  of 
vomiting  and  constipation,  and  because  be  was  inclined 
to  the  view  that  her  condition  was  due  to  diaphragmatic 
pleurisy  or  pneumonia. 

During  the  night  she  was  decidedly  worse ; the  abdo- 
men became  more  rigid  and  tender,  but  the  drawn 
anxious  expression  was  not  so  well  marked.  She  also 
vomited  three  times,  and  it  was  with  great  difficulty  that 
she  could  retain  any  food. 

On  the  morning  of  the  12th  Mr.  Dunn  saw  the  child 
with  me  again,  and  decided  to  operate.  The  abdomen 
was  opened  in  the  median  line,  and  general  peritonitis 
was  found.  There  was  a good  deal  of  slightly  turbid 
fluid  in  the  peritoneal  cavity,  and  the  intestines  were 
covered  with  flakes  of  pale  greyish-yellow  lymph.  The 
fluid  had  no  odour.  The  appendix  vermiformis  appeared 
to  be  a little  swollen,  and  it  was  removed.  A subsequent 
examination  showed  no  ulceration,  and  the  swelling  was 
no  more  than  could  be  accounted  for  by  the  peritonitis. 
It  was  certainly  not  the  primary  focus  of  the  peritonitis. 
The  peritoneal  cavity  was  washed  out,  and  a drainage- 
tube  was  left  in.  I examined  some  of  the  peritoneal 
fluid,  staining  some  cover-glass  preparations  with  Macono- 
chie’s  capsule  stain,  and  found  a number  of  capsulated 
diplococci,  which  I considered  were  pneumococci.  Cul- 
tures were  also  taken,  but  no  growth  resulted. 

After  putting  the  child  back  to  bed  the  pulse  became 
very  feeble,  and  stimulants  were  administered.  In  the 
afternoon  she  had  an  attack  of  profuse  diarrhoea,  which 
was  stopped  with  a starch  and  opium  enema  and  bismuth. 
As  the  pulse  did  not  improve  saline  enemata  and  in- 
fusions of  saline  solution  into  the  axillae  were  administered. 
During  the  night  she  became  very  restless,  and  continued 
so  all  the  following  morning.  She  died  suddenly  on  the 
afternoon  of  the  13th,  at  4.30  p.m.  < ' 

I made  the  post-mortem  examination  twenty-one  hours 
after  death.  Rigor  mortis  was  well  marked.  The  body 
was  rather  wasted  and  anaemic.  There  was  general 


PNEUMOCOCCAL  PERITONITIS. 


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acute  pleurisy,  both  lungs  being  covered  with  light 
greyish-yellow,  thin  recent  lymph.  There  was  a small 
quantity  of  thin,  slightly  turbid  serous  fluid  in  both 
pleural  cavities.  There  was  no  pneumonic  consolidation 
of  any  part  of  either  lung,  and  no  evidence  of  any 
commencing  pneumonia.  The  larynx,  trachea,  and 


bronchi  appeared  to  be  normal.  There  was  no  peri- 
carditis. The  heart  weighed  51  grammes;  it  was  healthy. 
The  arteries  were  normal.  There  was  general  acute 
peritonitis.  The  peritoneal  blood-vessels  were  congested. 


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PNEUMOCOCCAL  PERITONITIS. 


The  coils  of  intestine  were  adhering  to  each  other  by- 
means  of  pale  greyish-yellow  lymph.  In  the  pelvis  there 
was  a little  turbid  serous  fluid.  There  was  no  local 
lesion  to  account  for  the  peritonitis.  There  was  no 
ulceration  of  the  stomach,  duodenum,  or  small  or  large 
intestine.  The  condition  of  the  appendix  vermiformis 
has  already  been  mentioned.  There  was  no  suppuration 
of  any  of  the  abdominal  viscera.  The  liver  weighed  184 
grammes,  and  the  spleen  54  grammes  ; they  were  both 
normal.  The  kidneys  weighed  102  grammes,  and  were 
quite  normal. 

Cultures  were  taken  from  the  blood  in  the  right 
ventricle,  from  the  spleen,  and  from  the  pleural  and  peri- 
toneal cavities.  Pneumococci  were  found  in  pure  culture  in 
the  first  three,  and  with  staphylococci  in  the  last.  Micro- 
scopical preparations  from  these  sources  also  showed 
capsulated  diplococci.  Mr.  Pakes  examined  the  cultures 
and  cover-glass  preparations,  and  confirmed  the  opinion 
that  the  diplococci  were  pneumococci. 

Remarks. — The  cause  of  death  was  pneumoccal  septi- 
caemia, for  pneumococci  were  found  in  the  heart,  blood, 
spleen,  pleural  and  peritoneal  cavities.  The  question 
naturally  arises  as  to  the  source  and  channel  of  the 
infection.  There  was  no  obvious  primary  lesion  found  in 
any  part  of  the  body,  and  the  clinical  and  pathological 
evidence  pointed  to  the  peritoneum  as  the  first  structure 
to  be  attacked.  Did  the  pneumococci  first  gain  access  to 
the  peritoneum  through  the  alimentary  canal  and  cause 
acute  peritonitis,  and  then  infect  the  blood,  or  was  it  a 
primary  blood  infection,  the  peritoneum  being  the  first 
structure  to  be  attacked?  I have  brought  forward  this  case 
as  one  of  pneumococcal  peritonitis,  as  all  the  symptoms 
pointed  to  the  peritoneum  as  the  structure  to  be  first 
implicated,  there  being  no  indication  of  the  lungs  or 
pleura  being  involved  ; and  the  post-mortem  evidence  also 
corroborated  this  view,  for  the  morbid  changes  were  more 
marked  and  advanced  in  the  peritoneum  than  in  the 
pleura. 


PNEUMOCOCCAL  PERITONITIS. 


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The  case  I have  just  recorded  makes  the  third  which  I 
have  had  the  opportunity  of  investigating  during  the  last 
eighteen  months.  The  appearance  of  the  lymph,  and 
the  character  of  the  fluid,  and  the  clinical  history  in  each 
of  these  cases  reminded  me  very  forcibly  of  several  cases 
I had  seen  some  years  ago,  in  which  no  local  lesion  was 
found,  and  which  were  classified  under  the  vague  and 
unsatisfactory  heading  idiopathic  peritonitis.  I am 
of  opinion  that  a large  proportion,  if  not  all,  of  these 
so-called  cases  of  idiopathic  peritonitis  would  have  proved 
to  have  been  due  to  pneumococcal  infections  had  they 
been  examined  from  a bacteriological  point  of  view. 


PRINTED  BY  ADLARD  AND  SON, 
BARTHOLOMEW  CLOSE,  E.C.  ; 20,  HANOVER  SQUARE,  W.  ; 
AND  DORKING. 


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